Beyond Apoptosis Cellular Outcomes of Cancer Therapy

Addressing a major field of interest for oncologists, cell biologists, and other biomedical researchers, Beyond Apoptosis provides an overview of how different biological mechanisms of cell death, senescence and mitotic catastrophe stop the growth of tumor cells treated with anticancer agents.Written by internationally renowned contributors, this text includes:morphological illustrations, as well as a DVD containing documents and video clips from various time-lapse microscopic studies of cell death and mitotic catastrophethe role and limitations of apoptosis as a determinant of the toxicity of anticancer agentsalternative mechanisms of the antiproliferative actions of anticancer drugs and radiation, such as non-apoptotic cell death, cell senescence, and mitotic catastrophenon-apoptotic forms of cell death, such as necrosis, paraptosis, autophagic cell death, and othersmorphological and kinetic differences of the various forms of cell death

Historical Status of Apoptosis. Apoptosis as a Determinant of Tumor Progression and Radiation Damage to Normal Tissues. What Does the Clinical Data Tell Us About the Role of Apoptosis in Sensitivity to Cancer Therapy? Response of Solid Tumors to Cancer Therapy: How Relevant is Apoptosis? Section 2: Non-Apoptotic Cell Death Historical Studies of Various Forms of Programmed Cell Death. Historical Studies of Various Forms of Programmed Cell Death. Mechanistic Taxonomy of Cell Death Programs. Serine Proteases in Apoptotic Programmed Cell Death. Caspase-mediated Programmed Cell Death/Apoptosis. Autophagic Cell Death. The Cellular Decision Between Apoptosis and Autophagic Programmed Cell Death. PARP and AIF-dependant Programmed Cell Death. Paraptosis. Section 3: Tumor Senescence in Cancer Treatment. Cell Senescence and its Effects on Carcinogenesis and Tumor Progression. Tumor-suppressing Activities of Senescent Keratinocytes. Inducing Senescence in Cervical Cancer by Targeting Papillomavirus Oncogenes. Drug-induced Tumor Senescence in Tumor Cells. Regulators of Drug-Induced Senescence in Tumor Cells. Mechanisms of Drug-induced Senescence in a Transgenic Mouse Tumor. Chemotherapy-induced Senescence in Clinical Cancer. Section 4: Mitotic Catastrophe and Choosing the form of Death. Mitotic Catastrophe as a Response to DNA Damage in Interphase. How Microtubule-Targeting Agents Kill Cells. Modes of Cell Death by Anti-cancer Agents: The Crucial Importance of Dose. How Do Cells Die After Irradiation?: Time Lapse Studies with Cells in Culture.

IGOR B. RONINSON is Director of the Cancer Center, Ordway Research Institute, and Adjunct Professor at Albany Medical College, Rensselaer Polytechnic Institute, and State University of New York at Albany, Albany, NY, USA. Dr. Roninson received his Ph.D. in Biochemistry from the Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. He is a member of the American Association for Cancer Research and Associate Editor of several journals in the field of cancer. Dr. Roninson is an accomplished journal contributor, invited lecturer, and inventor. He has been honored with several awards, including the AACR Award for Meritorious Achievement in Cancer Research. His major fields of research are mechanisms of cancer drug resistance and sensitivity, cell senescence in cancer and aging, and drug target identification through functional genomics.J. MARTIN BROWN is Professor of Radiation and Cancer Biology, Stanford University, Palo Alto, California, USA. Dr. Brown obtained his Ph.D. in Radiation and Cancer Biology from Oxford University, Oxford, UK. He is active member of the American Association for Cancer Research and the Association for Radiation Research, and he serves as chair of the External Advisory Committee of Radiation Leukemogenesis NSCOR. Dr. Brown has received the Henry S. Kaplan Distinguished Scientist and other influential awards, such as the Radiation Research Society Failla Award. His major fields of interest and research are molecular determinants of tumor response to therapy, tumor hypoxia, hypoxic cytotoxins, gene therapy, DNA repair, and genomic instability.DALE E. BREDESEN is Director and CEO, Buck Institute for Age Research, Novato, and Adjunct Professor, The University of California, San Francisco, California, USA. Dr. Bredesen received his M.D. from Duke University Medical Center, Durham, North Carolina, USA. He has been the recipient of many awards, including the Arthur Cherkin Award for Research in N